TY - JOUR T1 - Simvastatin inhibits smoke-induced airway epithelial injury: implications for COPD therapy JF - European Respiratory Journal JO - Eur Respir J SP - 350 LP - 361 DO - 10.1183/09031936.00042512 VL - 42 IS - 2 AU - Benjamin B. Davis AU - Amir A. Zeki AU - Jennifer M. Bratt AU - Lei Wang AU - Simone Filosto AU - William F. Walby AU - Nicholas J. Kenyon AU - Tzipora Goldkorn AU - Edward S. Schelegle AU - Kent E. Pinkerton Y1 - 2013/08/01 UR - http://erj.ersjournals.com/content/42/2/350.abstract N2 - Chronic obstructive pulmonary disease (COPD) is the third leading cause of death. The statin drugs may have therapeutic potential in respiratory diseases such as COPD, but whether they prevent bronchial epithelial injury is unknown. We hypothesised that simvastatin attenuates acute tobacco smoke-induced neutrophilic lung inflammation and airway epithelial injury. Spontaneously hypertensive rats were given simvastatin (20 mg·kg−1 i.p.) daily for either 7 days prior to tobacco smoke exposure and during 3 days of smoke exposure, or only during tobacco smoke exposure. Pretreatment with simvastatin prior to and continued throughout smoke exposure reduced the total influx of leukocytes, neutrophils and macrophages into the lung and airways. Simvastatin attenuated tobacco smoke-induced cellular infiltration into lung parenchymal and airway subepithelial and interstitial spaces. 1 week of simvastatin pretreatment almost completely prevented smoke-induced denudation of the airway epithelial layer, while simvastatin given only concurrently with the smoke exposure had no effect. Simvastatin may be a novel adjunctive therapy for smoke-induced lung diseases, such as COPD. Given the need for statin pretreatment there may be a critical process of conditioning that is necessary for statins’ anti-inflammatory effects. Future work is needed to elucidate the mechanisms of this statin protective effect. ER -